Ultrastructural alterations of rat lung exposed to pyrolysis products of polytetrafluoroethylene (PTFE, Teflon).

Ultrastructural changes of the lung tissues were evaluated in rats exposed to the pyrolysis products of Teflon at 380 degrees C., 400 degrees C;, and 450 degrees C., respectively, for 4 hours. At 450 degrees C. Teflon evolved numerous tiny particles (0.02 to 0.04 mum.), which were considered to be the toxic material, and at 550 degrees C., in addition to the tiny particles, large spherical particles (0.7 to 5.0 mum) were found. No particles were observed in the pyrolysis product produced at temperatures between 380 degrees C. and 425 degrees C. There were no clinical symptoms or lung alterations induced at temperatures below 425 degrees C colloidal carbon injected as a marker of increased vascular permeability did not pass through the alveolar capillary endothelium. At 450 degrees C. (approximate lethal temperature) rats revealed severe respiratory difficulty, pulmonary edema, hemorrhage, and necrosis of the tracheobronchial epithelium. The membranous pneumocytes appear to be vulnerable to the Teflon fume causing cytoplasmic swelling, bleb formation, fragmentation, and denudation. Similar changes were found in the endothelial cells, but to a much lesser extent. When Teflon fume generated at 450 degrees CnWAS FILTERED THROUGH A Millipore filter (pore size 0.2 mum.), rats revealed only slight degenerative changes in the superficial tracheobronchial epithelium, but no clinical signs.

Experiments on the effect of carbon monoxide on aminolevulinic acid dehydrase (ALAD).

The inverse relationship between blood lead concentration and aminolevulinic acid dehydrase (ALAD) is well known. Recently, it has been suggested that a similar relationship exists between carboxyhemoglobin (COHb) and ALAD activity. This study was undertaken to examine more closely the possible effect of carbon monoxide on ALAD. Blood from 19 human volunteers was analyzed for both carboxyhemoglobin and ALAD activity. Smokers had significantly lower concentrations of ALAD than nonsmokers and a rise in carboxyhemoglobin concentration was assocaited with a fall in ALAD activity. The in vitro bubbling of carbon monoxide into human blood did not significantly effect ALAD activity. Four groups of rats (10 per group) wre exposed to carbon monoxide or dietary lead acetate according to the following design: (I) Control--no Pb or CO; (II) 500 ppm Pb acetate in diet; (III) 250 ppm CO four hours/day X 5 days/week X 4 weeks; (IV) Both Pb and CO. Analysis of the rat data showed a significant depression of ALAD by lead. The activity of ALAD in the rats exposed to CO was significantly increased suggesting the possibility of an adaptive phenomenon.